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      Impaired cognitive function and mental performance in mild dehydration

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      European Journal of Clinical Nutrition
      Springer Science and Business Media LLC

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          Abstract

          Dehydration is a reliable predictor of impaired cognitive status. Objective data, using tests of cortical function, support the deterioration of mental performance in mildly dehydrated younger adults. Dehydration frequently results in delirium as a manifestation of cognitive dysfunction. Although, the occurrence of delirium suggests transient acute global cerebral dysfunction, cognitive impairment may not be completely reversible. Animal studies have identified neuronal mitochondrial damage and glutamate hypertransmission in dehydrated rats. Additional studies have identified an increase in cerebral nicotinamide adenine dinucleotide phosphate-diaphorase activity (nitric oxide synthase, NOS) with dehydration. Available evidence also implicates NOS as a neurotransmitter in long-term potentiation, rendering this a critical enzyme in facilitating learning and memory. With ageing, a reduction of NOS activity has been identified in the cortex and striatum of rats. The reduction of NOs synthase activity that occurs with ageing may blunt the rise that occurs with dehydration, and possibly interfere with memory processing and cognitive function. Dehydration has been shown to be a reliable predictor of increasing frailty, deteriorating mental performance and poor quality of life. Intervention models directed toward improving outcomes in dehydration must incorporate strategies to enhance prompt recognition of cognitive dysfunction.

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          The changing landscape of ischaemic brain injury mechanisms.

          Thrombolysis has become established as an acute treatment for human stroke. But despite multiple clinical trials, neuroprotective strategies have yet to be proved effective in humans. Here we discuss intrinsic tissue mechanisms of ischaemic brain injury, and present a perspective that broadening of therapeutic targeting beyond excitotoxicity and neuronal calcium overload will be desirable for developing the most effective neuroprotective therapies.
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            Enhanced memory for emotional material following stress-level cortisol treatment in humans.

            Memory tends to be better for emotionally arousing information than for neutral information. Evidence from animal studies indicates that corticosteroids may be necessary for this memory enhancement to occur. We extend these findings to human memory performance. Following administration of cortisol (20 mg) or placebo, participants were exposed to pictures varying in emotional arousal. Incidental memory for the pictures was assessed one week later. We show that elevated cortisol levels during memory encoding enhances the long-term recall performance of emotionally arousing pictures relative to neutral pictures. These results extend previous work on corticosteroid enhancement of memory and suggest that high cortisol levels during arousing events result in enhanced memory in humans.
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              Role of dehydration in heat stress-induced variations in mental performance.

              Variation in mental performance under different levels of heat stress-induced dehydration was recorded in 11 subjects heat acclimatized to the tropicals. Dehydration was induced by a combination of water restriction and exercise in heat. The psychological functions--arithmetic ability, short-term memory, and visuomotor tracking--were assessed in a thermoneutral room after the subjects recovered fully from the effects of exercise in heat, as reflected by their oral temperature and heart rate. The results indicated significant deterioration in mental functions at 2% or more body dehydration levels.
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                Author and article information

                Journal
                European Journal of Clinical Nutrition
                Eur J Clin Nutr
                Springer Science and Business Media LLC
                0954-3007
                1476-5640
                December 2003
                December 18 2003
                December 2003
                : 57
                : S2
                : S24-S29
                Article
                10.1038/sj.ejcn.1601898
                14681710
                7c1df4df-c06f-434b-bc32-74ef4c80b9db
                © 2003

                http://www.springer.com/tdm

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